The cancer stem cell hypothesis suggests that neoplastic clones are maintained by a small sub-population of tumor cells with stem cell-like properties, and that these cells are responsible for tumor growth and invasiveness (Al-Hajj 2003; Dick 2003; Galli 2004; Hope 2004; Kondo 2004; Singh 2004; Gao 2005). Recently, the concept of “cancer stem cells” has gained more prominence, with increasing evidence to suggest the presence of a distinct subset of cells within the tumor mass that possess high potential for tumorigenicity and invasiveness (Bjerkvig 2005; Lahad 2005). The term “cancer stem cell” has been described operationally as a cancer cell that has the ability to self-renew by asymmetric cell division. Asymmetric cell division results in a second generation malignant stem cell and a cell that gives rise to the phenotypically diverse tumor cell population (Bjerkvig 2005). Tumor cells that combine the traits of stemness and mobility hold important clues for malignant progression (Brabletz 2005a; Brabletz 2005b). Tumor stem cells also have certain features that are common to normal stem cells, such as longer lifespan, higher proliferative potential and ability to migrate.
The abundance of cancer stem cells may vary within different tumors. Studies of myeloid leukemia, breast cancer, and brain cancers have described the defining characteristics of cancer stem cells (Al-Hajj 2003; Dick 2003; Hope 2004; Singh 2004). Cancer stem cells may be responsible for maintaining the malignant potential of a tumor, and may serve as the underlying cause of tumor recurrence. Current treatment strategies may miss targeting this distinct sub-population, and could explain initial therapeutic response and subsequent recurrence. Therefore, there is a need for methods of identifying and characterizing cancer stem cells, which will allow for the development of treatment methods that reduce or eliminate this critical cell population and thereby increase the effectiveness of various cancer therapies.